Comprehensive analysis of organic ligands in whole root exudates using nuclear magnetic resonance and gas chromatography-mass spectrometry

Hepatitis C virus (HCV) infection becomes persistent in the majority of instances in the face of a humoral and cellular immune response, and persistent HCV infection is associated with chronic hepatitis. In particular, cytotoxic T lymphocytes (CTL), crucial in the eradication of virus-infected cells, have been observed in the liver and the peripheral blood of chronically infected patients, suggesting that CTL cannot completely eliminate the virus, and may contribute to chronic liver injury. In this review, the potential host and the viral factors involved in the pathogenesis of chronic HCV infection will be discussed with emphasis on the HLA-A2 restricted peripheral blood CTL response and its relationship to liver disease and viral load.     

Enhancement of HBsAg detection in serum of patients with chronic liver disease following removal of circulating immune complexes

Patients with chronic liver disease and hepatocellular carcinoma may lack serological evidence of previous hepatitis B virus infection. The purpose of the present study was to test the hypothesis that circulating immune complexes may interfere with the detection of low levels of HBsAg in such patients. Sera from 190 patients were initially screened for the presence of circulating immune complexes. Patients belonged to three clinical categories: asymptomatic HBsAg carriers (50 patients), chronic liver disease (30 patients) and hepatocellular carcinoma (110 patients). Forty-one of the group of 190 patients (21%) were positive for circulating immune complexes. Sera from 21 patients were selected for further evaluation. The sera of 13 chronic liver disease or hepatocellular carcinoma patients (HBsAg negative, hepatitis B virus-DNA negative, with or without evidence of previous hepatitis B virus infection) and eight HBsAg positive carriers (four asymptomatic, three with chronic liver disease and one with hepatocellular carcinoma) were passed through a Clq affinity column (first column) to remove circulating immune complexes. Unbound material was then passed through a monoclonal IgG2a anti-HBs affinity column (second column). Unbound material (following both columns) contained free HBsAg, as determined by monocolonal radio-immunoassay, in eight patients in whom HBsAg had been undetectable in the original serum. Removal of circulating immune complexes from the serum of the three HBsAg positive patients with chronic liver disease also caused a significant increase in measurable circulating HBsAg compared with the original serum.(ABSTRACT TRUNCATED AT 250 WORDS)     

Correlations of C1q- and C3d-bearing circulating immune complexes with immunopathological disease activity in lupus nephritis patients

The serum levels of circulating immune complexes (CIC) measured by three different types of enzyme immunoassay (EIA) using monoclonal anti-C1q and antibodies and C1q as solid phase reagents were compared with clinical disease activity and immunohistological glomerular lesions in 29 SLE patients. Three types of CIC measured by these assays (anti-C1q CIC, anti-C3d CIC and C1q SP CIC) showed significantly higher levels in patients than in controls and were significantly associated with the clinical and serological disease activities. Anti-C1q CIC showed good correlation not only with mesangial IgG depositions (P < 0.01), but also with that of C1q (P < 0.05). C1q SP CIC also showed a weak correlation with mesangial C1q deposition (P < 0.05). Serum levels of anti-C3d CIC increased with the degree of mesangial IgG and complement depositions. Analysis of the clinical course of a patient with active SLE revealed a more rapid decrease of anti-C1q CIC and anti-C3d CIC along with the improvement of disease activity, including the mesangial lesion, than that of C1q SP CIC. According to these results, the CIC detected with assays using monoclonal antibodies against complement fragments, especially the anti-C1q assay, is likely to provide specific information regarding the clinical, serological and immunohistological disease activity in lupus nephritis.     

The immunological diagnosis of chronic viral hepatitis

Chronic viral diseases of the liver are associated with changes in immune reactions mediated by T and B lymphocytes and dependent in severity on etiological factor (virus of hepatitis B, delta, C, their combination), the disease stage (hepatitis, cirrhosis), the process activity, kind of immune correction. HBsAg, viral hepatitis B marker, was detected in 21.2% of 1400 cases with chronic active hepatitis and liver cirrhosis. 32% of HbsAg-seropositive patients had antibodies to delta-antigen. Antibodies to HBsAg, HCV were found in 27.7 and 14.9% of the above patients. Chronic viral diseases of the liver with persistence of HBV, HDV and HCV markers are characterized by a complex of immune disorders, including a moderate rise in peripheral blood of IgM, IgG, IgA, IgE, Ig kappa, lambda, immune complexes, cryoglobulins, autoantibodies to subcellular structures as well as changes in regulatory (suppressor, helper) and effector (lymphokine-producing) functions of T lymphocytes, inhibition of phagocytosing capacity. The above shifts in immune status, clinical and biochemical activity of the disease are more pronounced in chronic active hepatitis with HCV markers compared to BHV. Of maximal intensity they were in combined viral infection HBV+HDV or HBV+HCV.     

Intracellular accumulation of incompletely processed transforming growth factor-alpha polypeptides in ground glass hepatocytes of chronic hepatitis B virus infection

BACKGROUND: Transforming growth factor-alpha is an intracellularly processed and secreted polypeptide that induces a proliferative response in epithelial target cells and represents a potential regulatory factor in embryonic development, liver regeneration, and also hepatocarcinogenesis. We have observed focal transforming growth factor-alpha expression in liver tissues with chronic hepatitis B virus infection. METHODS: To further elucidate the nature of this focal transforming growth factor-alpha accumulation we have analyzed overall 23 different liver tissues with chronic hepatitis B virus and hepatitis C virus infection as well as normal liver tissues by immunohistology, ELISA, and Western immunoblot with and without immunoprecipitation. RESULTS: By immunohistology transforming growth factor-alpha polypeptides showed focal subcellular accumulation in ground glass hepatocytes, the histological hallmark of chronic hepatitis B virus infection, in co-localization with HBV-preS1 antigen. By ELISA and Western immunoblot increased tissue concentrations of transforming growth factor-alpha were demonstrated in chronically hepatitis B virus-infected liver tissues with ground glass hepatocytes, especially a 15-kD polypeptide, most likely representing an incompletely processed transforming growth factor-alpha polypeptide. Transforming growth factor-alpha retention in ground glass hepatocytes is not a general unspecific effect, since it was not observed for several other secretory liver proteins. Accumulated transforming growth factor-alpha in ground glass hepatocytes does not co-localize with Epidermal Growth Factor Receptor expression. CONCLUSION: Thus evidence is presented that a principally secreted (viral) polypeptide (HBV-preS1) can interfere with the secretion and processing of a second (cellular) protein (transforming growth factor-alpha). Accumulation of transforming growth factor-alpha may result from alteration of the endoplasmic reticulum due to storage of hepatitis B virus surface antigen particles. No evidence was found for transforming growth factor-alpha in ground glass hepatocytes to intracellularly interact with the Epidermal Growth Factor Receptor.     

A histopathological study of alcoholics with chronic HCV infection: comparison with chronic hepatitis C and alcoholic liver disease

To clarify the relationship between hepatitis C virus infection and excessive alcohol intake, we carried out histological examination of the liver in 46 alcoholics with chronic hepatitis C virus infection and compared the findings in 55 patients with chronic hepatitis C, 38 with alcoholic liver disease, and 27 with chronic hepatitis B. The majority of alcoholics with chronic hepatitis C virus infection displayed virus-related histological changes very similar to those in chronic hepatitis C, including frequent lymphoid follicles (34.7%) or aggregates (93.3%) in the portal tracts, mild necroinflammatory change (76.1%) in the parenchyma, and lymphocytosis in sinusoids (83.7%). Liver cell dysplasia and irregular regenerative activity of hepatocytes were rarely observed. The effects of alcohol on the liver were found to be minimal in the majority. These findings could suggest that the hepatic injury in the majority of alcoholics with chronic hepatitis C virus infection in Japan is due to persistent hepatitis C virus infection rather than to alcoholic injury. In addition, our study disclosed that the perivenular fibrosis which is designated as a histological characteristic of alcoholic liver disease is frequently observed in chronic hepatitis C. These similarities suggest that a similar fibrogenesis is present in chronic hepatitis C and alcoholic liver disease.     

Hepatitis G virus co-infection in liver transplantation recipients with chronic hepatitis C and nonviral chronic liver disease

Hepatitis G virus (HGV) is a newly described RNA virus that is parenterally transmitted and has been found frequently in patients with chronic hepatitis C infection. To determine the impact of hepatitis G virus co-infection on morbidity and mortality following liver transplantation, we measured HGV RNA by polymerase chain reaction in pre and posttransplantation sera from a cohort of patients transplanted for chronic hepatitis C and a control group of patients transplanted for nonviral causes who were negative for hepatitis C virus (HCV) RNA in serum. The overall prevalence rate of HGV RNA in transplanted patients with chronic hepatitis C was 20.7%. HGV infection was present before transplantation in 13% while it appeared to have been acquired at the time of transplantation in 7.4%. Mean serum alanine aminotransferase activity, hepatic histological activity, and patient and graft survival were similar between HGV-positive and HGV-negative patients. The prevalence rate of HGV RNA in transplanted controls was 64% (P < .01) with a significantly higher rate of acquisition of HGV infection following transplantation (53%, P < .001) when compared with patients with chronic hepatitis C. Mean serum alanine aminotransferase activity was significantly lower in the control patients with HGV infection alone following transplantation than in patients co-infected with hepatitis C (37 +/- 9 vs. 70 +/- 33 U/L, P < .01). Thus, HGV is frequently found in transplantation patients co-infected with hepatitis C although it appears to have minimal clinical impact. In patients transplanted for nonviral causes of end-stage liver disease, a high rate of hepatitis G acquisition at the time of transplantation may occur but does not appear to predispose to chronic hepatitis.     

Chronic hepatitis in children after liver transplantation: role of hepatitis C virus and hepatitis G virus infections

BACKGROUND/AIMS: Chronic graft hepatitis occurs in 20-30% adults after liver transplantation but the prevalence and causes in children are not known. In adults, hepatitis C virus infection is prevalent prior to transplantation and recurrent infection is a frequent cause of graft dysfunction. The significance of the recently described hepatitis G virus infection remains unproven. The aim of this study was to examine the role of hepatitis C virus and hepatitis G virus infection in chronic graft hepatitis after paediatric liver transplantation. METHODS: The prevalence of graft hepatitis and the role of hepatitis C virus and hepatitis G virus infections in 80 children after liver transplantation have been studied, with a median follow up of 4.4 years (range 0.4 to 10.7), and the persistence of hepatitis G infection in the presence of immunosuppression has been determined. RESULTS: Chronic graft hepatitis was diagnosed in 19/80 (24%) children and was most frequently seen in children transplanted for cryptogenic cirrhosis (71%). There was no significant difference in the prevalence of chronic hepatitis in those transplanted before or after donor anti-HCV screening. Hepatitis C infection occurred in three children transplanted prior to donor screening but in only one was associated with chronic hepatitis. Hepatitis G infection was found in 22/79 (28%) transplant recipients but was not associated with graft hepatitis. In 17/21 children hepatitis G infection persisted for a median of 5.2 years after transplantation. CONCLUSION: Chronic hepatitis occurred in 24% of children after liver transplantation, a similar prevalence to that in adults. Cryptogenic liver disease predisposed to graft hepatitis, but neither hepatitis C nor hepatitis G infection was associated. Hepatitis G virus caused a frequent and usually persistent infection after transplantation.     

Detection of the putative E2 protein of hepatitis C virus in human liver

The question was asked whether a predicted envelope protein, considered to be processed from the polyprotein precursor encoded by the putative E2/NS1 region of the hepatitis C virus (HCV) genome, may be observed in HCV-infected humans. Two polyclonal antibodies against recombinant E2/NS1 proteins were prepared and their reactivity tested against liver extracts from HCV-infected patients by immunoblotting analysis. A band corresponding to a size of 44 kDa was detected in liver extracts from patients who were positive for the HCV-specific antibody anti-C100-3 but not in liver extracts from patients who did not have anti-C100-3 antibody. Additionally, no band was detected using preimmune sera or antisera which had been preabsorbed with recombinant E2/NS1 proteins. Deglycosylation studies demonstrated that the 44 kDa protein was a glycosylated form of a 38 kDa protein which corresponds to the predicted molecular weight of the putative E2/NS1 protein. These results suggest that the 44 kDa protein is a product of the E2/NS1 region. Frequent observation of the 44 kDa band in cases of chronic active hepatitis C suggests a correlation between the expression of this protein and the progression of hepatitis.     

Consumption of alcohol in the presence of hepatitis C virus is an additive risk for liver damage

BACKGROUND: Whether alcohol consumption influences the development of hepatitis C in the presence of a latent infection needs to be determined. METHODS: The interaction between alcohol intake and hepatitis C virus infection with regard to development of liver injury was cross-sectionally investigated for 399 inhabitants of a town in Nagano Prefecture, Japan. In this town, the prevalence of hepatitis C virus infection is 32.4%. RESULTS: The levels of indicators of liver function were significantly higher among subjects of both sexes who carried the antibody to hepatitis C virus than among those without the antibody. Among men, higher levels of liver function were more frequent among alcohol drinkers than among nondrinkers, suggesting that alcohol consumption may aid in the development of liver injury, even among subjects with a latent hepatitis C virus infection. gamma-Glutamyl transpeptidase activity was more sharply increased in relation to alcohol intake among subjects with hepatitis C virus infection than among those without it, suggesting that the presence of infection will influence alcohol-induced liver damage. CONCLUSION: Alcohol consumption and a concomitant hepatitis C virus infection apparently facilitate the development of hepatitis.     

Overview of nuclides for bone pain palliation

Currently, six distinct types of hepatitis virus have been identified: A, B, C, D, E, and G. Hepatitis A virus infection does not cause a chronic carrier state, and perinatal transmission is extremely uncommon. Hepatitis B can be transmitted perinatally, but immunization of the newborn with hepatitis B immune globulin and hepatitis B vaccine markedly reduces the risk of neonatal infection. Hepatitis D virus is dependent on coinfection with the hepatitis B virus for replication. Immunoprophylaxis against hepatitis B also is effective against hepatitis D. Hepatitis C virus is primarily transmitted by the parenteral route and is particularly likely to cause chronic liver disease. Perinatal transmission of hepatitis C principally occurs in women who have high titers of HCV-RNA or who are coinfected with human immunodeficiency virus. At this time, no immunoprophylaxis for hepatitis C is available. Hepatitis G, a recently described organism, is related to hepatitis C. Its clinical significance remains undetermined. Hepatitis E is transmitted in a manner similar to hepatitis A. Perinatal transmission is unusual, but maternal disease is often severe.     

GB virus-C/hepatitis G virus infection in an area endemic for viral hepatitis, chronic liver disease, and liver cancer

BACKGROUND & AIMS: GB virus-C/hepatitis G virus (GBV-C/HGV) is a newly identified flavivirus, and little is known about its clinical significance. GBV-C/HGV was investigated in different populations, and its coinfection was investigated in patients with liver disease in Taiwan where hepatitis B and C are endemic. METHODS: Viral RNA was studied in 70 high-risk individuals, 20 patients with chronic non-B, non-C hepatitis, 13 with non-A-E fulminant hepatitis, 100 with asymptomatic hepatitis B surface antigen carriage, 120 with hepatitis B surface antigen-positive chronic liver disease and hepatocellular carcinoma, 100 patients with chronic hepatitis C, and 100 healthy adults. RESULTS: GBV-C/HGV infection was more frequent in high-risk groups (15%-30%) and hepatitis C virus carriers (10%) than in healthy adults (1%) and hepatitis B virus carriers (3.2%). Eighty-three percent of those infected had undergone blood transfusions previously. The prevalence in hepatitis B virus carriers increased with the severity of liver disease, being 1% in asymptomatic carriers and 10% in hepatocellular carcinoma. In chronic hepatitis C, clinical and virological data were comparable between those with and without coinfection. CONCLUSIONS: In Taiwan, GBV-C/HGV infection is common in high-risk groups, and its coinfection seems to not aggravate the course of chronic hepatitis B or C.     

Hepatitis C virus c100 antigen in liver tissue from patients with acute and chronic infection

A pool of murine monoclonal antibodies developed against c100 antigen, a hepatitis C virus-associated protein encoded by the NS3/NS4 virus genome, was used to detect hepatitis C virus in liver biopsy specimens from patients with acute and chronic hepatitis C virus infection. The antigen was present in the cytoplasm of liver cells only. The immunoreactive signal appeared as large, distinct, brilliant fluorescent granules with no clear relationship to cellular structures. No obvious membrane c100 antigen accumulation was observed. Distribution of c100-containing hepatocytes was directly correlated with viral replication in acute hepatitis. All three acute-hepatitis patients were positive for hepatitis C virus RNA (as detected on polymerase chain reaction) in serum and displayed c100 antigen in 50% to 70% of hepatocytes, with a distinct topographical relationship with necrotic areas and inflammatory cell accumulation. Conversely, very low numbers of infected cells and no relationship between tissue c100 antigen expression and sites of liver cell necrosis and inflammation were found in 14 chronic hepatitis C virus infection patients. Furthermore, though all patients had measurable levels of serum hepatitis C virus RNA, only eight (57%) had detectable c100 antigen in liver sections. Indeed, these two distinct immunopathological patterns were inversely related to the development of c100 antibody in serum. Specificity of hepatocellular c100 antigen deposits was established through extensive absorption experiments using structural and nonstructural hepatitis C virus recombinant proteins. However, tissue processing was found to be a crucial step in the demonstration of hepatitis C virus antigen in fresh frozen liver tissue.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical applications of registration and fusion of multimodality brain images from PET, SPECT, CT, and MRI

The aim was to assess the specificity and functional significance of liver-infiltrating and peripheral blood T cells in chronic hepatitis C. Peripheral blood mononuclear cells hepatitis C virus from 50 of 58 (86.2%) patients with chronic hepatitis C virus infection and 6 of 28 (21.4%) controls showed a proliferative T cell response to at least one of 16 synthetic peptides covering highly conserved regions of the core, envelope (El) and non-structural regions (NS4) of hepatitis C virus. However, six immunodominant peptides were exclusively recognized by the proliferating blood mononuclear cells from 46 patients with chronic hepatitis C virus infection (79.3%). Fine specificity and HLA-restriction were studied with 15 peptide-specific CD4+ T cell lines and 23 T cell clones isolated from liver tissue and peripheral blood of 12 patients with chronic hepatitis C. It was demonstrated that the peptide-specific response of CD4+ T cells was restricted to the presence of autologous accessory cells and HLA-DR and -DP molecules. Eight peptide-specific T cell lines and five T cell clones derived from liver tissue and peripheral blood, released interferon-gamma (200-6600 pg/ml) and tumor necrosis factor-alpha (100-400 pg/ml) and no or little interleukin-4 (< 140 pg/ml) after peptide-specific or mitogeneic stimulation, thus resembling a Th1-like cytokine profile. Patients with active liver disease showed significantly higher proliferative responses to hepatitis C virus core peptides than asymptomatic hepatitis C virus carriers or complete responders to interferon therapy. In conclusion, class II-restricted CD4+ T cell responses to some immunodominant epitopes within the hepatitis core region correlated with disease activity in chronic hepatitis C virus infection. Functionally, liver-infiltrating and peripheral blood T cells released Th1-like cytokines in response to the specific stimulus. Thus, it can be suggested that CD4+ T cells can mediate the pathogenesis of chronic hepatitis C virus induced liver disease.     

Chronic non-B, non-C hepatitis among blood donors assessed with HCV third generation tests and polymerase chain reaction

Forty five blood donors with increased serum aminotransferases levels had liver histologic assessment and were tested for antibodies to hepatitis C virus (anti-HCV) with second and third generation ELISAs and RIBAs, and for HCV RNA with polymerase chain reaction (PCR) in serum and liver tissue. Twenty-nine of these 45 donors (65%) had steatosis without chronic hepatitis. Sixteen (35%) had chronic hepatitis. Twelve had evidence of HCV infection. Four had no evidence of HCV infection demonstrable by ELISA, RIBA or PCR. These four patients had no known cause of chronic hepatitis and no risk factor for parenterally acquired viral infection was found in them. This observation supports the hypothesis that a non-B, non-C virus might be implicated in chronic hepatitis. However, this hypothesis remains to be demonstrated.     

Alcoholism, hepatitis B and C viral infections, and impaired liver function among Taiwanese aboriginal groups

Viral hepatitis and alcoholism prevail in four major Taiwanese aboriginal groups. To study the relative importance of the acquisition of hepatitis B virus or hepatitis C virus infection and alcoholism to the presence of impaired liver function in these groups, the authors conducted a semistructured clinical interview for alcoholism and test for seromarkers for viral hepatitis among 993 cohort members enrolled in 1990-1992 in an ongoing prospective study (Taiwan Aboriginal Study Project). The subjects' blood specimens were tested for serum alanine aminotransferase/aspartate aminotransferase levels and for the presence of hepatitis B surface antigen and anti-hepatitis C virus antibody. The prevalence of a combination of an alanine aminotransferase level of > 35 IU/liter and an aspartate aminotransferase level of > 40 IU/liter, implying impaired liver function or advanced liver disease, was 4.3% overall. Univariate and multiple logistic regression analysis showed that, rather than chronic hepatitis B virus infection, hepatitis C virus infection and alcoholism were the two dominant risk factors that signalled the risk of liver damage among these Taiwanese aborigines. In addition, these two contributing factors were able to act synergistically to cause impaired liver function.     

Chronic hepatitis C with normal aminotransferase levels: a clinical histologic study

OBJECTIVE: To define chronic hepatitis C virus (HCV) infection among patients with persistently normal aminotransferase levels (PNAL). DESIGN: Retrospective chart review of all patients encountered during 1-yr with positive hepatitis C antibody (anti-C100-3 ELISA), no alternative cause for their liver disease and PNAL for 6 or more consecutive months prebiopsy. Blinded review of liver histology. SETTING: Outpatient hepatology clinics of two academic centers. PATIENTS: Fifty patients with PNAL among 303 with hepatitis C. MEASUREMENTS: Epidemiologic profiles, reasons for seroscreening and confirmatory analyses were tabulated. Histology was reviewed and grading of inflammatory activity and stage of fibrosis was determined by protocol. RESULTS: Among 50 patients with PNAL, 35 (70%) were female, 34 (68%) had parenterally acquired HCV, 44 (88%) abstained (> 2 yr) from ethanol, all were HIV-negative and none pharmacologically immunosuppressed. HCV infection was uniformly confirmed by RIBA II or HCV-RNA assay. The mean level of HCV-RNA by quantitative PCR was 3.79 x 10(5) copies/ml (range, 500 to 1.8 x 10(6) copies/ ml) and by B-DNA, 53 x 10(5) copies/ml (range, 3.5-230 x 10(5) copies/ml). Traditional histoevaluation yielded chronic hepatitis ("active", n = 15; "persistent", n = 25), cirrhosis (n = 7), and normal histology (n = 3). Blinded protocol review of histology (inflammatory grade/fibrotic stage) revealed 0/0 (n = 4), 1/0 (n = 6), 2/0 (n = 17), 2/1 (n = 3), 2/4 (n = 1), 3/0 (n = 2), 3/1 (n = 6), 3/2 (n = 2), and 3/3 (n = 9). CONCLUSIONS: In chronic HCV infection, active inflammation, fibrosis, and variable circulating HCV-RNA levels may coexist with PNAL, particularly among female nondrinkers. Asymptomatic carriers with normal histology comprise 6 to 8% of chronic hepatitis C with PNAL. Management guidelines for this group of patients need to be developed.     

Occurrence of anti-C1q antibodies in IgA nephropathy

BACKGROUND: The pathogenic mechanisms and the antigens involved in the establishment and progress of IgA nephropathy are unknown. As antibodies against C1q have been reported to correlate with SLE nephritis, we analysed the occurrence of these antibodies in IgA nephropathy in order to investigate the possibility of pathogenetic similarities in these renal disorders. METHODS: The occurrence of IgA- and IgG anti-C1q antibodies (anti-C1q) were determined by ELISA in patients with IgA nephropathy (n = 36) and SLE nephritis (n = 37), diseases both known to be associated with circulating immune complexes. Levels of these antibodies were also determined in two other glomerular diseases, i.e. idiopathic membranous glomerulonephritis (n = 7) and minimal change disease (n = 2), in which circulating immune complexes are usually not present, and in 40 healthy controls. RESULTS: IgA anti-C1q was observed in increased titres in 11/36 of the patients with IgA nephropathy, in 2/37 of the patients with SLE nephritis (both with proliferative disease) and in 1/9 of the patients with membranous and minimal change disease (P < 0.001). Increased titres of IgG anti-C1q were observed in 1/36 of the patients with IgA nephropathy, in 17/37 of the patients with SLE nephritis and in 0/9 of the patients with membranous and minimal change disease (P < 0.001). There were no correlations between the levels of anti-C1q antibodies and clinical parameters such as degree of proteinuria, haematuria, or renal function. Nor was there any correlation to the concentration of C3a and the terminal complement complex (TCC) in patients with IgA nephropathy. CONCLUSIONS: The occurrence of anti-C1q antibodies in both IgA nephropathy and SLE nephritis, albeit of different predominating isotypes, indicates the possibility of a similar pathogenic mechanism involved in these renal disorders. The occurrence of IgA anti-C1q antibodies in patients with IgA nephropathy has to our knowledge not previously been reported.